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INTRODUCTION: The purpose of the study was to evaluate the thermal protection provided by a 2–3 mm surfing wet suit during at least two hours of fin diving in shallow water with a temperature of 16–20°C. We examined the effect of wearing the suit while diving in cold water on cognitive performance, muscle strength, and hand motor function. METHODS: Subjects were six male well-trained rebreather divers, 19–23 years old, acclimatised to cold. They attended the laboratory on three separate occasions, when we conducted the experiment at one of three temperatures, 16, 18, and 20°C. Core temperature (gastrointestinal system), skin temperature, oxygen consumption, and cold perception were evaluated during the test. Before and immediately after the dives, subjects performed a series of cognitive, manual dexterity, and muscle strength tests. RESULTS: Core temperature decreased by 0.35–0.81°C over the two hours at all three water temperatures. No subject reached a core temperature below 35°C. The decrease in upper body skin temperature during the two hour dive ranged between 5.97 and 8.41°C (P < 0.05). Two hours diving in 16–20°C water resulted in a significant increase in the time taken to perform the task of unlinking and reassembling four shackles (∼30% longer, P < 0.05). No effect was found on the cognitive or muscle strength tests. CONCLUSION: A 2–3 mm wet suit provides adequate thermal protection in trained and cold-acclimatised young males engaged in active diving in shallow water with a temperature of 16°C and above.

The greatest danger faced by divers who use oxygen-enriched gas mixtures is central nervous system oxygen toxicity (CNS-OT). CNS-OT is characterised by convulsions resembling grand-mal epileptic seizures, which may terminate in drowning and death. Elevated arterial levels of carbon dioxide (CO(2)) (hypercapnia) represent a major risk factor for CNS-OT when breathing hyperoxic gas mixtures. To reduce the risk of a diver being involved in a CNS-OT incident due to hypercapnia, candidates for combat diving are examined at our institute using a routine physiological training procedure, in which they are tested for CO(2) detection and retention. We present the case of a candidate for combat diving, who unexpectedly exhibited signs typical of CNS-OT while breathing pure oxygen under normobaric conditions with > 3 kPa inspired CO(2). Severe headache and nausea, as well as facial muscle twitching, appeared during one of these routine tests. Subsequent medical examination including neurological tests, magnetic resonance imaging and an electroencephalogram were unremarkable. To the best of our knowledge, an event such as this has never previously been published in the medical literature. We present a discussion of the case, and a review of the relevant literature regarding CO(2) as a risk factor for the development of CNS-OT

Central nervous system oxygen toxicity is a major risk in closed-circuit diving, and the risk increases with elevation of the inspired carbon dioxide (CO2). Mandatory tests for CO2 retention and detection are common practice at the Israel Naval Medical Institute, for the instruction and selection of combat divers at an advanced stage in their training. Read test is a simpler test of the ventilatory response to CO2. Positive correlation between parameters from Read and mandatory tests, enable conducting the test at an earlier stage in diving candidates. In the mandatory test, divers (n = 45) breathing various levels of CO2 in oxygen, and tested for the detection and retention of CO2 reported their sensations. In the Read test, we recorded end-tidal CO2 and ventilation in subjects as they rebreathed from rubber bag. The slope of ventilation was calculated as a function of end-tidal CO2. There was low correlation between any of the parameters from our test and the Read test. There was low insignific...

Performance and safety are impaired in employees engaged in shift work. Combat divers who use closed-circuit oxygen diving apparatus undergo part of their training during the night hours. The greatest risk involved in diving with such apparatus is the development of central nervous system oxygen toxicity (CNS-OT). We investigated whether the switch from day-to-night activity may be a risk factor for the development of CNS-OT using a diurnal animal model, the fat sand rat (Psammomys obesus). Animals were kept on a 12:12 light-dark schedule (6 a.m. to 6 p.m. at 500 lx). The study included two groups: (1) Control group: animals were kept awake and active during the day, between 09:00 and 15:00. (2) Experimental group: animals were kept awake and active during the night, between 21:00 and 03:00, when they were exposed to dim light in order to simulate the conditions prevalent during combat diver training. This continued for a period of 3 weeks, 5 days a week. On completion of this phase, 6-sulphatoxymelatonin (6-SMT) levels in urine were determined over a period of 24 h. Animals were then exposed to hyperbaric oxygen (HBO). To investigate the effect of acute melatonin administration, melatonin (50 mg/kg) or its vehicle was administered to the animals in both groups 20 min prior to HBO exposure. After the exposure, the activity of superoxide dismutase, catalase and glutathione peroxidase was measured, as were the levels of neuronal nitric oxide synthase (nNOS) and overall nitrotyrosylation in the cortex and hippocampus. Latency to CNS-OT was significantly reduced after the transition from day-to-night activity. This was associated with alterations in the level of melatonin metabolites secreted in the urine. Acute melatonin administration had no effect on latency to CNS-OT in either of the groups. Nevertheless, the activity of superoxide dismutase and catalase, as well as nitrotyrosine and nNOS levels, were altered in the hippocampus following melatonin administration. On the basis of these results, we suggest that a switch from diurnal to nocturnal activity may represent an additional risk factor for the development of CNS-OT. Utilizing a diurnal animal model may contribute to our understanding of the heightened risk of developing CNS-OT when diving with closed-circuit oxygen apparatus at night.

Background: Structural changes in the human body resulting from aging may affect the response to altered levels of O2 and CO2. An abnormal ventilatory response to a buildup of CO2 in the inspired air due to rebreathing may result in adverse effects, which will impair the individual's ability to function under stress. The purpose of this study was to evaluate the effect of age on the respiratory response to wearing an escape hood at rest and during mild exercise. Methods: Subjects were seven healthy, young adult males (20–30 years) and seven healthy, middle-aged males (45–65 years). Inspired CO2 and O2, breathing pattern (tidal volume [VT] and breathing frequency [F]), and mouth inspiratory and expiratory pressures, were measured at rest and during mild exercise (50 w) while wearing the CAPS 2000 escape hood (Shalon Chemical Industries and Supergum-Rubber and Plastic Technology, Tel Aviv, Israel). Findings: Resting inspired CO2 was higher in the middle-aged group compared with the young group (2.2...

The traditional method used to evaluate escape masks has been to examine the composition of the inspired gas, although arterial carbon dioxide (CO2) and oxygen (O2) would be more relevant physiological parameters. The recent development of reliable, fast-responding transcutaneous CO2 detectors makes it possible to evaluate arterial CO2 and O2 saturation. The CAPS 2000 escape mask was designed to protect the head and respiratory system from chemical or biological attack. The question arises of whether there might be a risk of dangerous hypoxia-hypercapnia in rebreathing from the mask because of leakage of the expired gas from the nose-cup into the hood, although theoretical considerations rule this out. We studied a worst case scenario.Nine subjects wore the CAPS 2000 for 15 minutes after removal of the inspiratory valves. A mass spectrometer and transcutaneous sensor were used to measure O2 and CO2, arterial O2 saturation, and arterial partial pressure of CO2 (PCO2).Blood oxygen saturation decreased from an initial value of 98.4% to 96.2% at 2 minutes, subsequently rising and stabilizing at a level similar to control. Subcutaneous PCO2 rose from the control level of 36 to 43 torr after 5 minutes, then decreased to 42 torr and stabilized at that level. Inspired PO2 dropped from 21% to 16% at 3 to 4 minutes, rose to 17% at 8 minutes, and stabilized thereafter. Inspired PCO2 rose to 3% in the first minute and continued to rise to 3.5% at 3 minutes, after which it slowly decreased to 3% and stabilized at that level.The transcutaneous CO2 detector provided a true indication of the physiological state of the subject, and these parameters are sufficient on their own for the evaluation of breathing masks. CO2 and O2 did not reach dangerous levels with the inspiratory valves removed from the CAPS 2000 mask.

It is commonly accepted that hyperbaric oxygen-induced seizures, the most severe manifestation of central nervous system oxygen toxicity, are harmless. However, this hypothesis has not been investigated in depth. We used apoptotic markers to determine whether cells in the cortex and hippocampus were damaged by hyperbaric oxygen-induced seizures in mice. Experimental animals were exposed to a pressure of 6 atmospheres absolute breathing oxygen, and were randomly assigned to two groups sacrificed 1h after the appearance of seizures or 7 days later. Control groups were not exposed to hyperbaric oxygen. Caspase 9, caspase 3, and cytochrome c were used as apoptotic markers. These were measured in the cortex and the hippocampus, and compared between the groups. Levels of caspase 3, cytochrome c, and caspase 9 in the hippocampus were significantly higher in the hyperbaric oxygenexposed groups compared with the control groups 1 week after seizures (p0.01). The levels of two fragments of caspase 9 in the cortex were higher in the control group compared with the hyperbaric oxygen-exposed group 1h after seizures (p0.01). Hyperbaric oxygen-induced seizures activate apoptosis in the mouse hippocampus. The reason for the changes in the cortex is not understood. Further investigation is necessary to elucidate the mechanism underlying these findings and their significance.

Introduction: In the sunken submarine, a breakdown in the power supply can disrupt the provision of fresh air and the absorption of CO 2 . A personal device based on a breathing mask and the soda lime canisters used in the submarine is proposed for CO 2 absorption. Methods: In an unmanned experiment, a breathing simulator provided a flow of air at 8.7 L · min ―1 and a carbon dioxide output of 20.9 L · h ―1 , which passed through either one or two 3.8-kg canisters of soda lime. In the manned experiment, four subjects wore the breathing mask, which was connected to two 3.8-kg canisters of soda lime placed in a bag, and remained for 24 h in a sealed hyperbaric chamber. They inspired the chamber atmosphere and expired via the canisters. Results: In the unmanned experiment, the concentration of CO 2 when a single canister was used reached 1 % after 8 h, 2% after 22 h, and 2.5% after 37 h. With two canisters connected in sequence, the concentration of CO 2 reached 1 % after 48 h, while the pressure at the entrance to the canisters did not exceed 0.7 cm H 2 O. In the manned experiment, the CO 2 concentration decreased over the first 12 h from its initial value of 1.3%, stabilizing during sleep at 0.75%. Discussion: The personal carbon dioxide absorption device lowered the ambient CO 2 level over a period of 24 h, and could maintain this level for a further 24 h. Keeping CO 2 at a low level has an advantage over the peaks of 3% obtained with absorbent LiOH curtains, where elevated pressure and increased PCO 2 may have an adverse effect on the survivors. Some of the crew can remain active without using the device, while the others do the job of clearing the carbon dioxide for the whole crew.

Elevated arterial Pco2 (hypercapnia) has a major effect on central nervous system oxygen toxicity in diving with a closed-circuit breathing apparatus. The purpose of the present study was to follow up the ability of divers to detect CO2 and to determine the CO2 retention trait after 1 year of active oxygen diving with closed-circuit apparatus. Ventilatory and perceptual responses to variations in inspired CO2 (range: 0–5.6 kPa, 0–42 Torr) during moderate exercise were assessed in Israeli Navy combat divers on active duty. Tests were carried out on 40 divers during the novice oxygen diving phase (ND) and the experienced oxygen diving phase. No significant changes were found between the two phases for the minimal mean inspired Pco2 that could be detected. The mean (with SD in parentheses) end-tidal Pco2 during exposure to an inspired Pco2 of 5.6 kPa (42 Torr) was significantly higher in the novice diving phase than in the experienced diving phase [8.1 kPa (SD 0.7), 62 Torr (SD 5) and 7.8 kPa (SD 0.6), 59 Torr (SD 4), respectively; P ≤ 0.001]. One year of shallow oxygen diving activity with a closed-circuit apparatus does not affect the ability to detect CO2 nor does it lead to increased CO2 retention; rather, it may even bring about a decrease in this trait. This finding suggests that acquiring experience in oxygen diving with a closed-circuit apparatus at shallow depths does not place the diver at a greater risk of central nervous system oxygen toxicity due to CO2 retention.

Oxygen toxicity of the central nervous system (CNS-OT) can occur during diving with oxygen-enriched gas mixtures, or during hyperbaric medical treatment. CNS-OT is characterised by convulsions and sudden loss of consciousness, which may be fatal in diving. Heat acclimation is known to provide cross-tolerance to various forms of stress in different organs, including the brain. We hypothesised that heat acclimation may delay the onset of CNS-OT in the rat. Male Sprague–Dawley rats were acclimated to an ambient temperature of 32 °C for 4 weeks. Rats in the control group were kept at 24 °C. Both groups were exposed to oxygen at 608 kPa. EEG was recorded continuously until the appearance of the first electrical discharge preceding clinical convulsions. CO2 production was measured simultaneously with the EEG. Latency to CNS-OT was measured and brain samples were taken for evaluation of heat shock protein 72 (HSP72) levels by Western blot analysis at the end of the acclimation period and during 4 weeks of deacclimation. Latency to CNS-OT was twice as long in the heat-acclimated rat, with insignificant changes in CO2 production. This prolongation continued for 2 weeks during deacclimation. There was a significant increase in the level of HSP72 following heat acclimation, with a subsequent decrease during deacclimation. We conclude that heat acclimation prolongs latency to CNS-OT in a way that does not involve changes in metabolic rate. During deacclimation there was a linear relationship between latency to CNS oxygen toxicity and the level of HSP72. A possible beneficial effect of HSP72 is discussed.

Findings regarding blood glucose level (BGL) on exposure to hyperbaric oxygen (HBO) are contradictory. We investigated the influence of HBO on BGL, and of BGL on latency to central nervous system oxygen toxicity (CNS-OT). The study was conducted on five groups of rats: Group 1, exposure to oxygen at 2.5 atmospheres absolute (ATA), 90 min/day for 7 days; Group 2, exposure to oxygen once a week from 2 to 6 ATA in increments of 1 ATA/wk, for a period of time calculated as 60% of the latency to CNS-OT (no convulsions); Group 3, exposure to 6 ATA breathing a gas mixture with a pO2of 0.21; Group 4, received 10 U/kg insulin to induce hypoglycemia before exposure to HBO; Group 5, received 33% glucose to induce hyperglycemia before exposure to HBO. Blood samples were drawn before and after exposures for measurement of BGL. No change was observed in BGL after exposure to oxygen at 2.5 ATA, 90 min/day for 7 days. BGL was significantly elevated after exposure to oxygen at 6 ATA until the appearance of convulsions, and following exposure to 4, 5, and 6 ATA without convulsions ( P < 0.01). No change was observed in BGL after exposure to 6 ATA breathing a gas mixture with a pO2of 0.21. Hypoglycemia shortened latency to CNS oxygen toxicity, whereas hyperglycemia had no effect. Our results demonstrate an influence of HBO exposure on elevation of BGL, starting at 4 ATA. This implies that BGL may serve as a marker for the generation of CNS-OT.

Central nervous system oxygen toxicity is a major risk in closed-circuit diving, and the risk increases with elevation of the inspired carbon dioxide (CO2). Mandatory tests for CO2 retention and detection are common practice at the Israel Naval Medical Institute, for the instruction and selection of combat divers at an advanced stage in their training. Read test is a simpler test of the ventilatory response to CO2. Positive correlation between parameters from Read and mandatory tests, enable conducting the test at an earlier stage in diving candidates. In the mandatory test, divers (n = 45) breathing various levels of CO2 in oxygen, and tested for the detection and retention of CO2 reported their sensations. In the Read test, we recorded end-tidal CO2 and ventilation in subjects as they rebreathed from rubber bag. The slope of ventilation was calculated as a function of end-tidal CO2. There was low correlation between any of the parameters from our test and the Read test. There was low insignificant correlation between any parameter from the Read test and detection or retention of CO2. We cannot use the Read test as a test for CO2 retention or detection at an earlier stage in diving candidates.

Central nervous system oxygen toxicity (CNS-OT) can occur in humans at pressures above 2 atmospheres absolute (ATA), and above 4.5 ATA in the rat. Pulmonary oxygen toxicity appears at pressures above 0.5 ATA. We hypothesized that exposure to mild HBO following extreme exposure might provide protection against CNS, but not pulmonary oxygen toxicity. We measured the activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX), and nitrotyrosine and nNOS levels in the brain and lung in the following groups: (1) Sham rats, no pressure exposure (SHAM); (2) Exposure to 6 ATA oxygen for 60% of latency to CNS-OT (60%LT); (3) Exposure to 6 ATA for 60% of latency to CNS-OT, followed by 20 min at 2.5 ATA for recovery (REC); (4) Exposure to 6 ATA for 60% of latency to CNS-OT, followed by 20 min at 2.5 ATA oxygen and a subsequent increase in pressure to 6 ATA until the appearance of convulsions (CONV); (5) Control rats exposed to 6 ATA until the appearance of convulsions (C). SOD and CAT activity were reduced in both brain and lung in the REC group. GPX activity was reduced in the hippocampus in the REC group, but not in the cortex or the lung. nNOS levels were reduced in the hippocampus in the REC group. Contrary to our hypothesis, no difference was observed between the brain and the lung for the factors investigated. We suggest that at 2.5 ATA and above, CNS and pulmonary oxygen toxicity may share similar mechanisms.

We examined the hypothesis that repeated exposure to non-convulsive hyperbaric oxygen (HBO) as preconditioning provides protection against central nervous system oxygen toxicity (CNS-OT). Four groups of rats were used in the study. Rats in the control and the negative control (Ctl-) groups were kept in normobaric air. Two groups of rats were preconditioned to non-convulsive HBO at 202 kPa for 1h once every other day for a total of three sessions. Twenty-four hours after preconditioning, one of the preconditioned groups and the control rats were exposed to convulsive HBO at 608 kPa, and latency to CNS-OT was measured. Ctl- rats and the second preconditioned group (PrC-) were not subjected to convulsive HBO exposure. Tissues harvested from the hippocampus and frontal cortex were evaluated for enzymatic activity and nitrotyrosine levels. In the group exposed to convulsive oxygen at 608 kPa, latency to CNS-OT increased from 12.8 to 22.4 min following preconditioning. A significant decrease in the activity of glutathione reductase and glucose-6-phosphate dehydrogenase, and a significant increase in glutathione peroxidase activity, was observed in the hippocampus of preconditioned rats. Nitrotyrosine levels were significantly lower in the preconditioned animals, the highest level being observed in the control rats. In the cortex of the preconditioned rats, a significant increase was observed in glutathione S-transferase and glutathione peroxidase activity. Repeated exposure to non-convulsive HBO provides protection against CNS-OT. The protective mechanism involves alterations in the enzymatic activity of the antioxidant system and lower levels of peroxynitrite, mainly in the hippocampus.

We have previously determined the thresholds for CO2 detection (conscious recognition of elevated CO2) and retention in male divers, beyond which a diving candidate should not continue his diving activity due to an increased risk of CNS oxygen toxicity. The purpose of the present study was to establish whether there is a difference in end tidal PCO2 between male and female divers who use oxygen-enriched gas mixtures. Ventilatory and perceptual responses to variations in inspired CO2 (range 0-42 mm Hg) were assessed during moderate exercise in 18 males and 18 females. End tidal PCO2 was lower in the female divers when breathing oxygen with 42 mm Hg CO2 (58.2±3.0 mm Hg vs. 61.5±4.5 mm Hg, P0.03). These results suggest that female divers have a lower end tidal CO2 than males when breathing a hyperoxic gas mixture during exercise, which might imply that women are less susceptible to CNS oxygen toxicity than men.

We have previously shown that heat acclimation provides protection against central nervous system oxygen toxicity (CNS-OT). This was well correlated with increased levels of heat shock protein 72 (HSP72). We now examine other antioxidative defenses against CNS-OT that are correlated with heat acclimation. Two groups of male Sprague-Dawley rats were used. The heat-acclimated group (HA) was exposed for 4 wk to 32°C, and the control group (C) was maintained at 24°C. At the end of the acclimation period, rats were exposed to oxygen at 608 kPa. EEG was recorded continuously until appearance of the first electrical discharge. Brain samples were taken from each group after exposure to pressure. Levels of the antioxidant enzymes CuZnSOD, MnSOD, catalase, and glutathione peroxidase, as well as levels of HSP72, were quantified by Western blot. Comparative proteome analysis of the brains of HA and C rats was carried out using two-dimensional electrophoresis and mass spectrometry to define protein spot alterations. Levels of HSP72 and CuZnSOD were higher in HA rats. Levels of the other antioxidant enzymes were not affected significantly by heat acclimation. Differences in the levels of four protein spots identified as α-synuclein, valosin-containing protein, adenylate kinase 1 (AK1), and the mitochondrial H+-ATP synthase α subunit were found between HA and C rats. We conclude that elevation of HSP72, CuZnSOD, AK1, and the mitochondrial H+-ATP synthase α subunit and possible phosphorylation of α-synuclein—all proteins involved in oxidative stress or energy conservation—might contribute to the prolongation of latency to CNS-OT induced by heat acclimation.

Many desert lizards show reduced rates of cutaneous water loss (CWL) compared to their counterparts from more humid environments. It is not clear yet whether reduced CWL is connected to the taxonomic position of the lizard studied, or is affected more by environmental or experimental conditions. To investigate this, we measured the skin resistance to water transfer, R s, in five closely related lizard taxa of the genus Agama. These diurnal lizards are distributed in Israel from mesic-Mediterranean to extreme desert biotopes. The highest R s (738 s cm-1) and the lowest CWL (0.160 mg cm-2 h-1) were found in Agama sinaita, which lives in the most arid habitat. The lowest R s (234 s cm-1) and the highest CWL (0.548 mg cm-2 h-1) were found in A. stellio ssp., which occupies mesic habitats. In addition, only the desert species were able to change their R s in accordance with the changing experimental conditions. These R s changes, which probably reflect vasomotor responses, were more pronounced in A. sinaita and presumably enable the desert species to control their CWL in a hot and dry environment.

Divers and patients lacking glucose-6-phosphate dehydrogenase (G6PD) may face a serious threat of central nervous system oxygen toxicity (CNS-OT) during exposure to hyperbaric oxygen (HBO), due to the important part played by G6PD in cellular redox balance. Our objective was to investigate G6PD deficiency as a risk factor for CNS-OT. We exposed G6PD-deficient (G6PDdef) and wild type (WT) mice to HBO at 405 kPa. Latency to CNS-OT was measured by observing the animal and monitoring the time to appearance of convulsions. Changes in glutathione peroxidase (GPx) and catalase activity were measured in red blood cells, and levels of endothelial and neuronal nitric oxide synthase (eNOS and nNOS) and 3-nitrotyrosine (NT) were measured in extracts of whole brain tissue by Western blot analysis. Unexpectedly, latency to CNS-OT was more than twice as long in G6PDdef mice compared with WT (36.9 ± 15.4 and 15.6 ± 13.2 min, respectively, P < 0.005). No significant differences were found in GPx and catalase activity or in protein levels of eNOS. However, nNOS and NT levels were lower in G6PDdef mice compared with WT (50.6%, P < 0.01 and 52.8%, P < 0.05, respectively). Our results suggest that the enhanced resistance of G6PDdef mice to HBO is due in part to a reduction in nNOS and NT levels in the brain. We conclude that G6PD deficiency at the level of the animals in the present study may not be a risk factor for developing CSN-OT, but this remains to be verified for human subjects.

Introduction: Contradictory results have been obtained regarding the beneficial effect of hyperbaric oxygen (HBO) on exercise performance. The purpose of this study was to investigate the effect of different combinations of pressure and time in hyperoxia on the energetic efficiency of trained and sedentary rats. Methods: At the end of the training period, rats were exposed to one of three protocols: 1) 100% normobaric oxygen for 24 h; 2) HBO at 2 ATA for 4 h; 3) HBO at 2.5 ATA for 6 h. After the hyperoxic exposures, V O2max was evaluated and compared with pre-exposure values. Results: The slope of the linear section of the oxygen consumption-velocity curve in the trained rats was significantly steeper after exposure to either 100% normobaric oxygen for 24 h or HBO at 2 ATA for 4 h than before the exposure. The opposite was found for the sedentary rats. After exposure to HBO at 2.5 ATA for 6 h, the slope of the oxygen consumption-velocity curve in the trained rats did not differ from the pre-exposure slope. However, the highest velocity these rats reached was lower than their maximum velocity before this exposure. In the sedentary rats, the slope of the oxygen consumption-velocity curve was found to be steeper after the 2.5 ATA exposure compared with the pre-exposure slope. Conclusions: Our results suggest that exposure to 100% normobaric oxygen for 24 h and HBO at 2 ATA for 4 h induces a reduction in the energetic efficiency of trained rats, but improves energetic efficiency in sedentary rats.

Elevated arterial PCO2 (hypercapnia) increases the risk of CNS oxygen toxicity when diving with enriched oxygen gas mixtures. A CO2 detection and retention test is conducted as a matter of routine at the Israel Naval Medical Institute for physiological training, and as a screening tool for divers who may be prone to suffer from CNS oxygen toxicity. This test does not include an "attention distracter", which would provide a better simulation of the true situation during actual diving. The purpose of the present study was to examine the hypothesis that the addition of cognitive tasks to the CO2 detection and retention test might alter divers' detection ability.We assessed ventilatory and perceptual responses to variations in inspired CO2 (range 0-5.6 kPa, 0-42 mmHg) during moderate exercise, with and without the addition of cognitive tasks, in 15 Israel Navy combat divers on active duty. The first stage was the CO2 detection training session, followed by the CO2 detection test session (TEST) and the CO2 detection test session while doing cognitive tasks (COGN). The latter two sessions were performed by some of the subjects in reverse order.We found that the mean (+/- SD) PICO2 at the detection threshold was significantly lower in the COGN (1.7 +/- 0.8 kPa, 12.7 +/- 6.0 mmHg) than in the TEST (2.4 +/- 0.6 kPa, 18.1 +/- 4.5 mmHg). The mean PETCO2 while inspiring 5.6 kPa (42 mmHg) CO2 was not significantly different in the two tests.We suggest that the ability to detect CO2 during a dive is not impaired, but rather improves when the diver's attention is focused on other tasks.

Several studies have been conducted in recent years in the attempt to improve running performance by the use of hyperbaric oxygen, but there is disagreement as to whether this has any beneficial effect. The purpose of this study was to measure the effect of 24 h breathing 100% O2 in normobaric conditions on energetic efficiency in the trained rat.Experiments were carried out on trained rats whose oxygen consumption was evaluated during the training period and on its completion. At the end of the training period, the rats were divided into two groups: 1) rats exposed to air (21% O2) in normobaric conditions; and 2) rats exposed to 100% O2 in normobaric conditions. In addition, two groups of sedentary rats were used: 3) sedentary rats exposed to air (21% O2) in normobaric conditions; and 4) sedentary rats exposed to 100% O2 in normobaric conditions. Energetic efficiency was estimated by measuring O2 consumption at submaximal exercise (45 m.min-1, 10 degrees incline).Training alone reduced O2 consumption by 18% during submaximal exercise. Exposure to 100% oxygen for 24 h in normobaric conditions reversed the effect of complete training by elevating the O2 consumption by 17%, which was close to the oxygen consumption of the rats during the incomplete training period.Our results suggest that prolonged exposure to hyperoxia induces a reduction in the energetic efficiency of the trained rat. The relevance of these findings to sports and diving is discussed.

Elevated arterial PCO2 (hypercapnia) is a known risk in diving with closed circuit breathing apparatus. In a retrospective study, we determined CO2 retention and the ability to detect CO2 in novice divers who were either CO2-recognition-trained subjects (TS) or untrained subjects (UTS).Ventilatory and perceptual responses to variations in inspired CO2 (range 0-5.6 kPa, 0-42 mm Hg) during moderate exercise were assessed in novice Israeli Navy divers on active duty. Tests were carried out on 231 TS and 213 UTS.The minimal mean inspired PCO2 that could be detected was 4.8 +/- 1.6 kPa (36 +/- 12 mm Hg) in UTS and 2.9 +/- 0.7 kPa (22 +/- 5 mm Hg) in TS (p0.0001). No significant changes were found in PETCO2 between the two groups during exposure to a PICO2 of 5.6 kPa (42 mm Hg). There were 46 TS who were found to be CO2 retainers (more than +1 SD above the mean) and 19 were classified as poor detectors (more than +1 SD above the mean). Seven subjects exhibited both traits. During actual oxygen diving performed later by this group, the only four cases of CNS-oxygen toxicity were among those seven subjects (p0.01).We conclude that CO2 recognition training improves the diver's capability to detect CO2. We suggest that a diver who is both a poor CO2 detector and a CO2 retainer will be prone to CNS-oxygen toxicity.

Based on our observations of energy sparing in heat-acclimated (AC) rat hearts, we investigated whether changes in preischemic glycogen level, glycolytic rate, and plasma thyroxine level mediate cardioprotection induced in these hearts during ischemia-reperfusion insults. Control (C) (24°C), AC (34°C, 30 days), acclimated-euthyroid (34°C + 3 ng/ml l-thyroxine), and control hypothyroid (24°C + 0.02% 6- n-propyl-2-thiouracil) groups were studied. Preischemic glycogen was higher in AC than in C hearts [39.0 ± 8.5 vs. 19.2 ± 4.2 (SE) μmol glucose/g wet wt; P < 0.0006], and the lactate produced vs. glycogen level during total ischemia (13C-NMR spectroscopy) was markedly slower (AC: −0.82 x, r = 0.98 vs. C: −4.7 x, r = 0.9). Time to onset of ischemic contracture was lengthened, and the fraction of hearts experiencing ischemic contracture was lowered. Pulse pressure recovery was improved in AC compared with C animals before, but not after, absolute sodium iodoacetate-induced glycolysis inhibition. Acclimated-euthyroid hearts exhibited decreased ischemic tolerance, whereas induced hypothyroidism in C improved cardiotolerance. Thus higher preischemic glycogen and slowed glycolysis are associated with hypothyroidism and are likely important mediators of the improved ischemic tolerance exhibited by AC hearts.